The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval

Recent evidence suggests repeated mild brain trauma may result in cumulative damage. We investigated cell damage and death in hippocampal cultures following repeated mechanical trauma in vitro by measuring propidium iodide (PrI) uptake, release of neuron-specific enolase (NSE) and glial S-100β prote...

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Main Authors: Jennifer E. Slemmer, John T. Weber
Format: Article
Language:English
Published: Elsevier 2005-04-01
Series:Neurobiology of Disease
Subjects:
NSE
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996104002335
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spelling doaj-ba3729a2f11242289c8378a7df44f8d22021-03-20T04:50:23ZengElsevierNeurobiology of Disease1095-953X2005-04-01183421431The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury intervalJennifer E. Slemmer0John T. Weber1Department of Neuroscience, Erasmus Medical Center, PO Box 1738, 3000 DR Rotterdam, The NetherlandsCorresponding author. Fax: +31 10 408 9459.; Department of Neuroscience, Erasmus Medical Center, PO Box 1738, 3000 DR Rotterdam, The NetherlandsRecent evidence suggests repeated mild brain trauma may result in cumulative damage. We investigated cell damage and death in hippocampal cultures following repeated mechanical trauma in vitro by measuring propidium iodide (PrI) uptake, release of neuron-specific enolase (NSE) and glial S-100β protein, and performing neuronal counts. Cultures receiving two mild injuries (31% stretch) 1 or 24 h apart displayed different profiles of PrI uptake and S-100β release, although neuronal loss and NSE release was similar in both paradigms. Cells receiving a subthreshold, low-level stretch (10%) repeated several times eventually stained with PrI. Cultures administered 10% stretch before mild injury released less S-100β than mild injury alone, suggesting a preconditioning effect. Lastly, exogenous S-100β applied to injured cultures decreased PrI uptake, implying a protective role. These results suggest cumulative damage is dependent on injury severity and inter-injury interval, and that neurons and glia react differently to various injury paradigms.http://www.sciencedirect.com/science/article/pii/S0969996104002335GliaIn vitro injuryNSERepetitive injuryS-100βTraumatic brain injury
collection DOAJ
language English
format Article
sources DOAJ
author Jennifer E. Slemmer
John T. Weber
spellingShingle Jennifer E. Slemmer
John T. Weber
The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval
Neurobiology of Disease
Glia
In vitro injury
NSE
Repetitive injury
S-100β
Traumatic brain injury
author_facet Jennifer E. Slemmer
John T. Weber
author_sort Jennifer E. Slemmer
title The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval
title_short The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval
title_full The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval
title_fullStr The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval
title_full_unstemmed The extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval
title_sort extent of damage following repeated injury to cultured hippocampal cells is dependent on the severity of insult and inter-injury interval
publisher Elsevier
series Neurobiology of Disease
issn 1095-953X
publishDate 2005-04-01
description Recent evidence suggests repeated mild brain trauma may result in cumulative damage. We investigated cell damage and death in hippocampal cultures following repeated mechanical trauma in vitro by measuring propidium iodide (PrI) uptake, release of neuron-specific enolase (NSE) and glial S-100β protein, and performing neuronal counts. Cultures receiving two mild injuries (31% stretch) 1 or 24 h apart displayed different profiles of PrI uptake and S-100β release, although neuronal loss and NSE release was similar in both paradigms. Cells receiving a subthreshold, low-level stretch (10%) repeated several times eventually stained with PrI. Cultures administered 10% stretch before mild injury released less S-100β than mild injury alone, suggesting a preconditioning effect. Lastly, exogenous S-100β applied to injured cultures decreased PrI uptake, implying a protective role. These results suggest cumulative damage is dependent on injury severity and inter-injury interval, and that neurons and glia react differently to various injury paradigms.
topic Glia
In vitro injury
NSE
Repetitive injury
S-100β
Traumatic brain injury
url http://www.sciencedirect.com/science/article/pii/S0969996104002335
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